title: Dietary camphene attenuates hepatic steatosis and insulin resistance in mice.
abstract: OBJECTIVE
  The aim of this study was to investigate the protective effects of camphene on high-fat diet (HFD)-induced hepatic steatosis and insulin resistance in mice and to elucidate its mechanism of action.
  
  
  METHODS
  Male C57BL/6N mice were fed with a normal diet, HFD (20% fat and 1% cholesterol of total diet), or HFD supplemented with 0.2% camphene (CPND) for 10 weeks.
  
  
  RESULTS
  Camphene alleviated the HFD-induced increases in liver weight and hepatic lipid levels in mice. Camphene also increased circulating adiponectin levels. To examine the direct effects of camphene on adiponectin secretion, 3T3-L1 adipocytes were incubated with camphene. Consistent with in vivo result, camphene increased adiponectin expression and secretion in 3T3-L1 adipocytes. In HFD-fed mice, camphene increased hepatic adiponectin receptor expression and AMP-activated protein kinase (AMPK) activation. Concordant with the activation of adiponectin-AMPK signaling, camphene increased hepatic expression of fatty acid oxidation-related genes and decreased those of lipogenesis-related genes in HFD-fed mice. Moreover, camphene increased insulin-signaling molecules activation and stimulated glucose transporter-2translocation to the plasma membrane in the liver.
  
  
  CONCLUSIONS
  These results suggest camphene prevents HFD-induced hepatic steatosis and insulin resistance in mice; furthermore, these protective effects are mediated via the activation of adiponectin-AMPK signaling.
authors.affiliation: Department of Food and Nutrition, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul, 120-749, South Korea.
authors.forename: Sohee
authors.initials: S
authors.lastname: Kim
authors.forename: Youngshim
authors.initials: Y
authors.lastname: Choi
authors.forename: Seoyoon
authors.initials: S
authors.lastname: Choi
authors.forename: Yeji
authors.initials: Y
authors.lastname: Choi
authors.forename: Taesun
authors.initials: T
authors.lastname: Park
mesh_terms: D041721:3T3-L1 Cells; D055372:AMP-Activated Protein Kinases / Q000737:chemistry / Q000378:metabolism*; D052438:Adipocytes, White / Q000378:metabolism / Q000473:pathology; D050156:Adipogenesis; D052242:Adiponectin / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use; D000081008:Bicyclic Monoterpenes; D019587:Dietary Supplements; D004789:Enzyme Activation; D005234:Fatty Liver / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D005786:Gene Expression Regulation; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009929:Organ Size; D011897:Random Allocation; D054419:Receptors, Adiponectin / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013729:Terpenes / Q000378:metabolism / Q000627:therapeutic use*
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; D000975:Antioxidants; D000081008:Bicyclic Monoterpenes; D054419:Receptors, Adiponectin; D013729:Terpenes; C475419:adiponectin receptor 1, mouse; C475421:adiponectin receptor 2, mouse; D055372:AMP-Activated Protein Kinases; C019286:camphene